What Causes Colon Cancer?

Colon cancer is a disease that develops in the lining of the large intestine, one of the most important parts of the digestive system, and is generally silent. The absence of symptoms in the early stages can make diagnosis difficult; therefore, understanding the causes of the disease is crucial for both prevention and raising awareness. In this article, we will examine the causes of colon cancer in light of scientific data.

What Are the Main Causes of Colon Cancer?

Colon cancer begins with the accumulation of damage to the genetic structure of the cells in the colon. Scientific research indicates that a high-fat and low-fiber diet, long-term inflammatory bowel diseases, and certain inherited gene mutations offer fundamental explanations for the cause of colon cancer.

Cell Mutations and Genetic Disruptions

The main cause of colon cancer is genetic mutations in the DNA of cells. When these mutations affect the genes that control cell growth, healthy cells begin to proliferate uncontrollably.

In particular, alterations in genes such as APC, KRAS, TP53, SMAD4, and TGF-β RII play a significant role in the development of colon cancer. Damage to these genes prevents cell cycle arrest and accelerates tumor development. Inherited syndromes such as Familial Adenomatous Polyposis (FAP) and Lynch Syndrome (HNPCC) are rare but high-risk examples of these mutations present at birth (Markowitz, Dawson, Willis & Willson, 2002).

Cancer Development from Colon Polyps

Colon cancer also arises from benign growths called adenomatous polyps that develop in the colon. These polyps are initially harmless, but if DNA damage accumulates over time, the cell structure deteriorates and can become cancerous.

This process is called the “adenoma-carcinoma sequence.” Activation of the Wnt signaling pathway in polyp tissue (e.g., resulting from APC or β-catenin mutations) is observed in the early stages, while additional mutations in the K-RAS and p53 genes accelerate cancer progression in later stages. Therefore, early detection and removal of polyps through colonoscopy is critical for preventing colon cancer (Greenwald, 1992).

The Role of Chronic Inflammation (Colonitis, Ulcerative Colitis)

Long-term inflammatory bowel diseases are a significant risk factor for the development of colon cancer. Ulcerative colitis and Crohn’s disease, in particular, lead to a continuous cycle of damage and regeneration in the intestinal wall. This chronic inflammation weakens DNA repair mechanisms and leads to the accumulation of cellular mutations. Research shows that inflammation accelerates cell division and increases the production of free radicals. Therefore, regular monitoring and appropriate treatment of chronic bowel diseases is one of the most effective measures against the cause of bowel cancer.

Lifestyle-Related Risk Factors

Colon cancer is closely linked not only to genetics but also to our daily habits. One of the answers to the question of what causes colon cancer is that certain lifestyles incorporate habits that negatively impact intestinal health. Diet, physical activity level, and duration of exposure to harmful substances constitute the most concrete explanations for the cause of colon cancer.

Low-Fiber Diet and Red Meat Consumption

Scientific studies show that diets low in fiber and high in red meat increase the risk of colon cancer. Fiber regulates bowel movements and shortens the contact time of potential carcinogens with the intestinal wall; therefore, inadequate fiber intake predisposes to cell damage.

Conversely, high-fat and red meat-rich diets increase bile acids, creating cellular stress in the colon mucosa. Nitrate and heterocyclic amine compounds, particularly those found in processed meats, can accelerate the process of cancer by triggering DNA mutations (Greenwald, 1992). Therefore, a diet rich in vegetables, fruits, and whole grains is one of the most effective measures to reduce the risk of colon cancer.

The Effects of Alcohol and Smoking on the Colon

Alcohol and smoking have a toxic effect on colon tissue, as well as the entire digestive system. Acetaldehyde, formed during alcohol metabolism, damages DNA structure and disrupts cell renewal. Nitrosamines and polyaromatic hydrocarbons in cigarette smoke increase the risk of mutations in the intestinal mucosa.
Studies have shown that the incidence of colon cancer increases by 20–40% in people who regularly consume alcohol, while this rate is even higher in smokers.

The Relationship Between Obesity and Sedentary Lifestyle and Cancer Risk

Obesity not only leads to metabolic disorders but also to increased inflammation at the cellular level. Excess fat tissue triggers insulin resistance and increased levels of growth factor (IGF-1), triggering uncontrolled proliferation in colon cells.

Furthermore, a sedentary lifestyle slows bowel movements and causes waste to stay in contact with the colon wall for longer periods of time. This process increases the risk of DNA damage and can accelerate the process of cancer. Regular physical activity is one of the most effective protective factors for maintaining a healthy weight and reducing inflammation.

The Impact of Genetics and Family History

Colon cancer is a disease that can develop not only through lifestyle and environmental factors but also through genetic inheritance. Family history is one of the strongest factors in determining an individual’s risk of colon cancer. Inherited mutations in certain genes, in particular, weaken cells’ DNA repair mechanisms, predisposing them to cancer development. This explains the genetic dimension of the question of what causes colon cancer.

Familial Colon Cancer Syndromes

Approximately 5–10% of colon cancer cases are caused by familial syndromes. In these syndromes, individuals are born with mutations in certain genes, and these mutations lead to uncontrolled cell proliferation.

One of the most well-known examples is Familial Adenomatous Polyposis (FAP). In this condition, hundreds or even thousands of polyps develop due to mutations in the APC gene, and the risk of developing colon cancer at an early age is close to 100%.

Another example is Lynch Syndrome (HNPCC). In this syndrome, DNA mismatch repair (MMR) genes—specifically MLH1, MSH2, and MSH6—are mutated. These mutations prevent cells from repairing DNA damage and quickly lead to cancer development (Markowitz, Dawson, Willis & Willson, 2002).

BRCA, Lynch Syndrome, and Other Inherited Mutations

Recent studies have shown that not only classic colon cancer genes but also genes responsible for DNA repair, such as BRCA1 and BRCA2, may influence colon cancer risk.

Microsatellite instability (MSI), observed in Lynch Syndrome, increases the mutation rate of cells by a thousandfold. This “mutator phenotype” mechanism is one of the key factors accelerating the process of cancer. In addition, inherited mutations in the TGF-β RII, SMAD4, KRAS, and TP53 genes also cause cell cycle disruption.

Early Age Risk in First-Degree Relatives

The risk of developing colon cancer increases two to threefold in individuals with a first-degree relative, such as a parent, sibling, or child, with a history of colon cancer. Early screening is crucial, especially if these cases are diagnosed under age 50.

Research shows that family history reflects a combination of both genetic and environmental factors. When similar dietary habits, lifestyle, and genetic predispositions come together, the answer to the question of what causes colon cancer becomes clearer: hereditary risk factors once again emphasize the importance of early diagnosis and regular screening (Markowitz, Dawson, Willis & Willson, 2002).

Environmental and Metabolic Triggers

Everyday exposure to foods, chemicals, and hormonal imbalances can predispose to DNA damage in intestinal cells and, in the long term, tumor development. Therefore, the question of what causes colon cancer is closely linked not only to hereditary factors but also to environmental triggers.

The Effect of More Processed Foods on Intestinal Flora

Highly processed and refined foods can accelerate the process of colon cancer by disrupting the balance of intestinal flora. Foods containing sugar, additives, and preservatives lead to a decrease in beneficial bacteria and an increase in harmful bacteria. This creates low-grade chronic inflammation in the intestine, triggering cellular stress and DNA damage.

A low-fiber diet, in particular, reduces the production of short-chain fatty acids (e.g., butyrate); these compounds, which normally provide energy for colon cells and have anti-inflammatory effects, are eliminated. When this protective mechanism is eliminated due to fiber deficiency, the gut microbiota is disrupted.

Chemical Exposures and Toxic Substances

Certain chemicals in the environment can increase the risk of colon cancer. Pesticides, heavy metals, and industrial solvents, in particular, induce mutations in cell DNA and disrupt repair mechanisms. Furthermore, toxic substances such as nitrosamines in tobacco smoke and polyaromatic hydrocarbons (PAHs) found in air pollution increase the oxidative damage accumulated in the colon mucosa. Long-term exposures of this type reduce the regenerative capacity of the intestinal epithelium, unbalance cell division, and increase the risk of colon cancer.

The Effect of Vitamin D Deficiency on Colon Health

Vitamin D is a critical molecule not only for bone health but also for the growth and differentiation processes of colon cells. Recent academic research has shown that vitamin D deficiency may increase the risk of colon cancer.

Vitamin D regulates apoptosis (programmed cell death) and DNA repair mechanisms in cells; in its deficiency, these processes are disrupted, and cells begin to proliferate abnormally.

A large-scale study conducted by the Harvard T.H. Chan School of Public Health reported that the risk of colon cancer increases by up to 30% in individuals with low serum 25(OH)D levels (Song et al., BMJ, 2019).

Underlying Factors that Trigger Colon Cancer

In addition to genetic predisposition and environmental factors, some often-overlooked underlying triggers play a role in the development of colon cancer. While factors such as an imbalance in the gut microbiota, long-term stress, or sleep disorders may not directly cause DNA damage, they can accelerate the cancer process by weakening the body’s defenses.

Disruption of Microbiota Balance (Dysbiosis)

The trillions of bacteria living in our intestines play an important role in regulating the immune system and maintaining cellular homeostasis. However, antibiotic use, a low-fiber diet, and processed foods disrupt this balance. This condition is called dysbiosis.

The increase in harmful bacteria resulting from dysbiosis can lead to the accumulation of toxic metabolites in the intestine and DNA damage in epithelial cells. Specifically, Fusobacterium nucleatum and Bacteroides fragilis species have been detected in high concentrations in colon tumor tissues and trigger inflammation, increasing cell proliferation (Greenwald, 1992).

Chronic Stress and Immune Weakness

Long-term stress reduces the immune system’s ability to recognize and destroy cancer cells. The stress hormones cortisol and adrenaline create oxidative stress in the body, which can lead to inflammation in the intestinal mucosa.

Furthermore, chronic stress affects the microbiota via the enteric nervous system, increasing the risk of dysbiosis. As the immune system weakens, cell repair slows and mutation rates increase. Clinical observations show that stress management and psychological support programs positively impact the treatment process in colon cancer patients.

Sleep Disorders and Hormonal Effects

Sleep patterns directly impact the body’s hormonal balance and cellular repair processes. It has been found that the risk of colon cancer increases, particularly in people who work night shifts or whose melatonin rhythm is disrupted.

The melatonin hormone regulates not only the sleep cycle but also the antioxidant defense system. Insufficient sleep reduces melatonin levels, making cells vulnerable to oxidative damage. One study reported a 35% increased risk of colon cancer in women who work long night shifts (Schernhammer et al., Journal of the National Cancer Institute, 2003).

Becoming aware of colon cancer is one of the most valuable steps you can take for your health. However, having reliable information, accurate guidance, and an experienced healthcare team are just as important. QBA Medi Tours communicates directly with specialist doctors in Cuba to create the most appropriate treatment plan for you and manages the entire process in a transparent, safe, and comfortable manner. Early diagnosis, correct treatment, and We stand with you in the fight against colon cancer with a holistic health approach. Don’t put off your health—contact us today to learn about advanced treatment options in Cuba and begin your journey to recovery with confidence.

Don’t put off your health; early diagnosis and proper treatment are critical in the fight against colon cancer. To discuss safe and comfortable treatment options with expert doctors in Cuba, please visit our Cuban Health Consulting and Cancer Treatment pages.

If you’d like to better understand modern treatment approaches for colon cancer, you can also review our article, “Differences Between the Cuban Cancer Vaccine and Immunotherapy.” This guide will help you better understand the role of immune-based treatments in colon cancer.

References

Markowitz, S. D., Dawson, D. M., Willis, J., & Willson, J. K. V. (2002). Focus on colon cancer. Cancer Cell, 1(3), 233–236. doi:10.1016/S1535-6108(02)00053-3

Greenwald, P. (1992). Colon cancer overview. Cancer, 70(S1), 1206–1215. https://doi.org/10.1002/cncr.2820700205

Song, M., et al. (2019). Vitamin D and colorectal cancer risk: An international pooling project of 17 cohorts. BMJ, 363:k4022. doi:10.1136/bmj.k4022

Schernhammer, E. S., Laden, F., Speizer, F. E., et al. (2003). Night-shift work and risk of colorectal cancer in women participating in the Nurses’ Health Study. J Natl Cancer Inst, 95(11), 825–828. doi:10.1093/jnci/95.11.825